With increasingly severe air pollution, the aggravated health risks of particulate matter, especially ultrafine particles, are emerging as an urgent and sensitive topic. Considering the heterogeneity and complexity of ultrafine particles, there is insufficient evidence about their toxic effects and possible molecular mechanisms. To address this question, we analyzed the emission characteristics of quasi-ultrafine particles collected during winter in a typical coal-burning city, Taiyuan, and confirmed their contribution to lung cancer cell adhesion and metastasis. For the specific mechanism, we revealed that the endocytosis of quasi-ultrafine particles stimulated the release of HMGB1, induced NFκB-facilitated proinflammatory cytokine production through the interaction of HMGB1 with RAGE, and resulted in cancer-endothelial cell adhesion. These findings remind us of the potential effects of anthropogenic quasi-ultrafine particle pollution and provide a theoretical reference for the mitigation of tumorigenesis in a severe particulate matter contaminated environment.

Coliform mastitis is a worldwide serious disease of the mammary gland. Curcumin is a pleiotropic polyphenol obtained from turmeric, but it is hydrophobic and rapidly eliminated from the body. However, nanoformulation of curcumin significantly improves its pharmacological activity by enhancing its hydrophobicity and oral bioavailability. Our study aimed to investigate the possible antioxidant and anti-inflammatory effects of nanocurcumin as a prophylactic against LPS-induced coliform mastitis in rat model, where LPS was extracted from a field strain of Escherichia coli (bovine mastitis isolate). The study was conducted on twenty lactating Wistar female rats divided into four equal groups, and the mastitis model was initiated by injection of LPS through the duct of the mammary gland. The results showed that nanocurcumin significantly attenuated the lipid peroxidation (MDA), oxidized glutathione, the release of pro-inflammatory cytokines (TNF-α and IL-1β), and the gene expression of TLR4, NF-κB p65, and HMGB1. Meanwhile, it improved the reduced glutathione level and Nrf2 activity and preserved the normal alveolar architecture. These findings suggested that nanocurcumin supplementation can be a promising potential protective approach for coliform mastitis.

Exposure to road dust particulate matter (PM) causes adverse health impacts on the human airway. However, the effects of road dust on the upper airway epithelium in humans remain unclear. We investigated the involvement of the epidermal growth factor receptor (EGFR) after PM with an aerodynamic diameter of < 2.5 μm (PM₂.₅)-induced E-cadherin disruption of human pharyngeal epithelial cells. First, we collected road dust PM₂.₅ from 10 Chinese cities, including Wuhan, Nanjing, Shanghai, Guangzhou, Chengdu, Beijing, Lanzhou, Tianjin, Harbin, and Xi’an. Human pharyngeal FaDu cells were exposed to road dust PM₂.₅ at 50 μg/mL for 24 h, cytotoxicity (cell viability and lactate dehydrogenase (LDH)) was assessed, and expressions of the proinflammatory interleukin (IL)-6 and high-mobility group box 1 (HMGB1) protein, receptor for advanced glycation end products (RAGE), occludin, E-cadherin, EGFR, and phosphorylated (p)-EGFR were determined. The E-cadherin gene was then knocked down to investigate EGFR activation in FaDu cells. Exposure to road dust PM₂.₅ resulted in a decrease in cell viability and increases in LDH and IL-6. Our data suggested that PM₂.₅ could decrease expressions of occludin and E-cadherin and increase expressions of EGFR and p-EGFR, which was confirmed by E-cadherin-knockdown. Our results showed a negative association between the alterations in E-cadherin and total elemental components in correlation analysis, especially S, Cl, K, Ti, Mn, Fe, Cu, Zn, and Pb. Exposure to metals in PM₂.₅ from road dust may lead to loss of the barrier function of the upper airway epithelium and activation of the EGFR. Our study showed the adverse effects of road dust PM₂.₅ on pharyngeal epithelial cells of the human upper airway.